MEMBRANE PHYSICAL STATE CONTROLS THE SIGNALING MECHANISM OF THE HEAT-SHOCK RESPONSE IN SYNECHOCYSTIS PCC-6803 - IDENTIFICATION OF HSP17 AS A FLUIDITY GENE

The fluidity of Synechocystis membranes was adjusted in vivo by temper ature acclimation, addition of fluidizer agent benzyl alcohol, or cata lytic lipid hydrogenation specific to plasma membranes, The reduced me mbrane physical order in thylakoids obtained by either downshifting gr owth temperature or administration of benzyl alcohol was paralleled wi th enhanced thermosensitivity of the photosynthetic membrane, Simultan eously, the stress-sensing system leading to the cellular heat shock ( HS) response also has been altered, There was a close correlation betw een thylakoid fluidity levels, monitored by steady-state 1,6-diphenyl- 1,3,5-hexatriene anisotropy, and threshold temperatures required for m aximal activation of all of the HS-inducible genes investigated, inclu ding dnaK, groESL, cpn60, and hsp17, The causal relationship between t he pre-existing thylakoid physical order and temperature set point of both the transcriptional activation and the de novo protein synthesis was the most striking for the 17-kDa HS protein (HSP17) associated mos tly with the thylakoid membranes, These findings together with the fac t that the in who modulation of lipid saturation within cytoplasmic me mbrane had no effect on HS response suggest that thylakoid acts as a c ellular thermometer where thermal stress is sensed and transduced into a cellular signal leading to the activation of HS genes.